When Bacteria Kill Us, It's More Accident Than Assassination - Aeon Essays

7/11/2021 When bacteria kill us, it’s more accident than assassination | Aeon Essays
Coincidental killers
We assume that microbes evolved to attack
humans when actually we are just civilian
casualties in a much older war
A colorized transmission electron micrograph of Escherichia coli bacteria. Photo courtesy Elizabthe H White/CDC
Ed Yong is an award-winning science writer, whose work has appeared in The New
Yorker, National Geographic, Wired, the New York Times, Nature and New Scientist,
among others. He is currently a staff writer for The Atlantic. His latest book is I Contain
Multitudes: The Microbes Within Us and a Grander View of Life (2016).
https://aeon.co/essays/when-bacteria-kill-us-it-s-more-accident-than-assassination?utm_source=Aeon+Newsletter&utm_campaign=52b0d09b63-EMAIL_CAMPAIGN_2… 1/8
The classic novel by H G Wells, The War of the Worlds (1898) – a tale of England
besieged by Martian conquerors – ends not with a rousing and heroic victory but an
accidental one. The aliens subjugate humanity with heat rays and black smoke but, at
the height of their victory, they die. Their machines come to a standstill amid the
ruins of a deserted London, and the birds pick at their rotting remains. The cause of
their downfall? Bacteria. As the novel’s unnamed narrator says, they were ‘slain, after
all man’s devices had failed, by the humblest things’.
Wells’s logic was simple. Humans have immune systems that protect us from the
infectious germs that we’ve been exposed to since our earliest origins. We still get
diseases, but at least we can put up a fight. The Martians, despite their technological
superiority, could not. ‘There are no bacteria in Mars,’ the narrator explains, ‘and
directly these invaders arrived, directly they drank and fed, our microscopic allies
began to work their overthrow.’
When I first read the book about two decades ago, this final twist seemed like a cop-
out. It comes out of nowhere – a sort of deus ex microbia rescue – and, besides,
Earth’s microbes could not possibly grow in an alien body. But more recently, I have
come to realise that Wells, writing at the close of the 19th century, was inadvertently
hinting at a truth about bacteria that even today’s microbiologists sometimes forget:
these organisms can become lethal through evolutionary accidents.
In the novel, bacteria did not evolve to cripple the aliens. They evolved to target
humans and other animals. The invaders unexpectedly stepped into the crossfire, and
succumbed. The same can happen to us. Many of the bacteria and fungi that afflict us
with severe diseases are not aiming at us at all. Instead, they have evolved to thrive in
harsh environments or to fend off other microbes. It just so happens that these same
adaptations allow them to thrive in our bodies or to fend off our immune systems.
Consider Streptococcus pneumoniae, a common bacterium that lives in our noses and
airways. It is typically harmless but it can sometimes flip from passive passenger to
active killer, causing pneumonia, meningitis, sepsis, and other illnesses. This typically
happens in people with weakened immune systems, and it’s often the fault of strains
that have thick coats of complex sugar molecules that protect them from our immune
systems.
But in 2007 Elena Lysenko, then at the University of Pennsylvania School of

Medicine, found that there is more to this story than strong microbe meets
compromised host. S.pneumoniae shares our airways with other bacteria such as
Hemophilus influenzae. These species do not make for happy neighbours, and
H.influenzae has been known to marshal its host’s white blood cells to attack its
competitor. This strategy usually works. When Lysenko incubated the two microbes
together in mice, she found the rodents usually ousted S.pneumoniae from their
airways, leaving H.influenzae to rule alone.
But the thickly armoured strains of S.pneumoniae are impervious to white blood cells,
and can stand their ground. Their armour would normally be a liability – they take so
much energy to make that their owners get outcompeted by strains that make lighter
and less costly coats. But with H.influenzae mobilising an immune army, a thick coat
suddenly becomes worthwhile. And by coincidence, those coats make these strains
better at invading deeper parts of the respiratory system, and causing serious disease.
In defending itself from a competitor, S.pneumoniae inadvertently becomes an
armoured killer.
Its virulence – its ability to cause disease – is not an adaptation against its host. It is a
side effect, a fluke. It kills through coincidence.
In the late 17th century, the Dutch scientist Antonie van Leeuwenhoek created a new
type of microscope lens and brought an entire world of tiny organisms into focus.
Looking at his own dental plaque, he wrote: ‘I then most always saw with great
wonder, that in the said matter there were many very little living animalcules, very
prettily a-moving.’ These little creatures were intriguing but seemingly unimportant,
and few others picked up the baton from van Leeuwenhoek. That changed in the
19th century, when Louis Pasteur and Robert Koch proved that some of these
microbes were behind important diseases.
That framing has stuck. Microbes are everywhere, but we take their presence on
phones, keyboards, and toilet seats as a sign of filth and squalor. They fill our bodies,
helping us to digest our food and safeguard our health, but we view them as
adversaries to be drugged and conquered.
This antagonism is understandable. Aside from those of us with access to

microscopes, most people will never see microbes with their own eyes. And so we
tend to identify microbes with the disease-causing minority among them, the little
buggers that trigger the tickling mist of a sneeze or the pustule on otherwise smooth
skin. We become aware of their existence when they threaten our lives, and for much
of our history, that threat was substantial. Epidemics of smallpox, cholera,

tuberculosis, and plague have traumatised humanity, and the fear of these diseases
has contaminated our entire culture, from our religious rites to Hollywood films such
as Contagion (2012) or Outbreak (1995).
When microbes aren’t killing us, we are largely oblivious to them. So, we construct
narratives of hosts and pathogens, heroes and villains, us and them. Those that cause
disease exist to reproduce at our expense, and we need new ways of resisting them.
And so we study how they evolve to outfox our immune system or to spread more
easily from one person to another. We identify genes that allow them to cause disease
and we label those genes as ‘virulence factors’. We place ourselves at the centre of
their world. We make it all about us.
We might think of antibiotics as modern

inventions, but they’re actually weapons that
bacteria have been using against each other for
aeons
But a growing number of studies show that our anthropocentric view is sometimes
unjustified. The adaptations that allow bacteria, fungi and other pathogens to cause
us harm can easily evolve outside the context of human disease. They are part of a
microbial narrative that affects us, and can even kill us, but that isn’t about us. This
concept is known as the coincidental evolution hypothesis or, as the Emory
University microbiologist Bruce Levin described it in 2008, the ‘shit happens’
hypothesis.
This hypothesis does not apply to all infections, and is almost certainly irrelevant to
viruses, which always need to reproduce in a host. Nor does it apply to the many
bacteria and fungi, such as Staphylococcus aureus or Candida albicans, that are long-
standing human pathogens and well-adapted to us. But it does explain some weird
aspects of many diseases.
Why, for example, would bacteria harm the hosts that they depend on for survival? In
some cases, the answer is obvious: they cause symptoms such as sneezing or
coughing that help them to spread. But what about S.pneumoniae? Strains that sit
harmlessly in a host’s airways are already capable of spreading to another individual.
The virulent forms, which descend deeper into the respiratory tract, are actually less
contagious. The same goes for bugs such as Hemophilus influenzae and Neisseria
meningitidis, which can inflame the protective membranes around the brain and lead
to life-threatening cases of bacterial meningitis. In doing so, they risk capsizing their
own ship without any hope of boarding a new one.
The coincidental evolution hypothesis helps to resolve these paradoxes. It tells us that
at least some human diseases have nothing to do with us at all.
The coincidental evolution hypothesis explains a number of other recent discoveries

about microbes. Scientists have found antibiotic resistance genes in bacteria that
have been frozen for 30,000 years, or isolated in million-year-old caves. We might
think of antibiotics as modern inventions, but they’re actually weapons that bacteria
have been using against each other for aeons, or at least well before Alexander
Fleming noticed a funky mould in a Petri dish in 1928. Antibiotic resistance genes
evolved as part of this ancient war, but they also help today’s microbes to deal with
the medicines that we mass-produce.
Likewise, many of the ‘virulence genes’ that help pathogens to cause disease have
counterparts in marine microbes with no track record of infecting humans. And
some supposedly pathogenic bacteria were often common parts of the environment.
‘These organisms become accidental pathogens,’ says the microbiologist Arturo
Casadevall from Yeshiva University in New York. ‘They’ll still be there even if you
remove all the animals from the planet. And yet, evolution selected for just the right
combination of traits to cause disease in humans.’
We fear lions and tigers and bears; bacteria have

to contend with phage viruses, nematode worms,
and predatory amoebas
Vibrio cholerae, the bacterium that causes cholera, is a good example. Scientists used
to regard it as a human pathogen that spreads when the faeces of infected people
seep into water supplies. We now know that it’s mainly a marine species that attaches
itself to the shells of small crustaceans, and occasionally makes its way into our water
supply. ‘In the last decade, people have begun to accept that a lot of these
opportunistic pathogens that people assumed were only in the environment
transiently between human hosts are actually environmental bacteria that

occasionally end up in humans,’ says Diane McDougald from the University of New
South Wales, who studies V.cholerae.
Many of the pathogens we fear most are mere tourists on the human body. Their real
homes are oceans, caves, or soils. To understand them, we need to understand them
within their natural ecology. Soil, for example, is an extreme habitat for a microbe:
harsh and constantly changing. It can quickly oscillate from flood to drought, from
scalding heat to freezing cold, and total darkness to intense solar radiation. It’s rife
with other competing microbes, and crawling with hungry predators. We fear lions
and tigers and bears; bacteria have to contend with phage viruses, nematode worms,
and predatory amoebas.
All of these conditions can lead to adaptations that make microbes accidentally
suited for life in a human host. We are, after all, just another environment. A thick
capsule that shields a microbe from dehydration could also shield it from our
immune system. A spore that is adapted for travelling through the air can be easily
inhaled into a respiratory tract.
Scientists have demonstrated many of these coincidental adaptations by exposing

bacteria to a natural threat and showing that they then become better at infecting
humans and other mammals. Escherichia coli, for example, is a common gut
bacterium, and a darling of laboratory scientists. In its natural environments, whether
the soil or the gut of a mammal, it is menaced by predatory amoebas, which threaten
to engulf and digest it. In 2010, the French scientist Frantz Depaulis and colleagues
found an E.coli strain called 536 that resists these predators, with genes that protect it
from the amoebas’ digestive enzymes and allow it to scavenge nutrients such as iron.
Rather than being disintegrated, it actually grows inside its would-be predator and
eventually kills it from within.
Many of these protective genes also allow strains of the mostly harmless E.coli to
cause severe illness in humans, mice and other mammals. This makes perfect sense.
Many of our immune cells, like macrophages, engulf and digest microbes just as
amoebas do, so an amoeba-proof bacterium is also a macrophage-proof one. By
adapting to their natural predators, strains of E.coli are coincidentally pre-adapted to
foil our immune system.
The coincidental evolution hypothesis might be irksome to some. What are the odds
that an adaptation to one challenge would perfectly predispose an organism to
another? The answer, it seems, is: pretty high. Evolution, however, is all about small
probabilities manifesting through long timescales and large numbers – and microbes
have both. They have been living on the planet for billions of years, and there are
countless legions of them.
Casadevall likes to say that each microbe holds a different hand of cards –
adaptations that allow it to cope with its environment. Most of these combinations
are meaningless to us. A bacterium might be able to resist being digested by other
cells, but it might not be able to grow at 37 degrees Celsius. It might grow at the right
temperature, but it might not be able to tolerate our slightly alkaline pH levels. But
that doesn’t matter. There are so many microbes out there that some of them will end
up with a hand that lets them muscle their way into our game. ‘If you take all the
microbial species in the world and imagine that they have these traits randomly, you
can find pathogenic microbes for practically anything,’ says Casadevall.
we’re not central actors in the dramas that affect

our lives. We are just passers-by
This inevitability paints the rise of new infectious diseases in a new light. The past few
decades have seen the rise of terrifying new fungi, such as the chytrid fungus that is
massacring the world’s amphibians, or the one behind the White-nose syndrome that
has killed millions of North American bats. ‘People ask where these came from,’ says
Casadevall. ‘It may just be that their virulence was generated by selection forces that
have nothing to do with the hosts they ended up with.’
The same rationale explains why human explorers should be cautious if we ever
encounter a planet with microbial life. ‘Most people in infectious disease think that if
there are microbes in Mars, what do we have to worry about?’ says Casadevall. ‘They
won’t have the right proteins for causing diseases in humans. But if you had enough
microbes, there might be pathogens there.’
If that’s the case, these infections might continue being virulent for a long time.
‘When I was a student, parasitologists would tell you that disease was a primitive
state in the relationship between a parasite and its host,’ says Levin. ‘Everyone
eventually evolves to niceness and co-operation, with symbiosis and mutualism as the
endpoints.’ But if virulence is coincidental to begin with, there might not be much of
an evolutionary pressure for the inadvertent pathogen to change its ways.
There is something unsatisfying, almost nihilistic, about this idea. It deprives us of

answers. As Casadevall wrote in a review, it says that virulence can arise by chance,
‘in a process that has no explanation, except for that it happened’. According to this
outlook, we’re not central actors in the dramas that affect our lives. We’re not even bit
players. We are just passers-by, walking outside the theatre and getting hit by flying
props.
The most important parts of a microbe’s world are, after all, other microbes. They’ve
been dealing with each other for billions of years before we came along. When we
step into the crossfire of this ancient war, we risk becoming collateral damage. Like
Wells’s Martians, we too can be laid low by coincidence.
aeon.co 1 January 2014

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7/11/2021 When bacteria kill us, it’s more accident than assassination | Aeon Essays

But in 2007 Elena Lysenko, then at the University of Pennsylvania School of

This antagonism is understandable. Aside from those of us with access to

of our history, that threat was substantial. Epidemics of smallpox, cholera,

We might think of antibiotics as modern

The coincidental evolution hypothesis explains a number of other recent discoveries

We fear lions and tigers and bears; bacteria have

transiently between human hosts are actually environmental bacteria that

Scientists have demonstrated many of these coincidental adaptations by exposing

we’re not central actors in the dramas that affect

There is something unsatisfying, almost nihilistic, about this idea. It deprives us of

aeon.co 1 January 2014

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